EEG basics and sleep
Download
Report
Transcript EEG basics and sleep
EEG basics and sleep
John O’Donovan
Consultant old age psychiatrist
Hans Berger
Another first for psychiatry
First recorded EEG in 1924
The first rhythm he saw was
called the alpha rhythm
Interesting man, originally a
mathematics student who wanted
to be an astromoner
Switched to medicine in an
attempt to explain personal belief
in telepathy
Was a psychiatrist during WW1
Ended up collaborating with the
NAZIs and committed suicide at
68 years of age.
EEG
Principles
• The brain functions via electricity and
chemistry.
• The electricity in the form of post synaptic
inhibitory and excitatory potentials can be
recorded from the scalp and analysed.
• Stunning temporal resolution but poor spatial.
• Cortical rhythms tend to be driven via deeper
brain structures in particular the intralaminar
nuclei of the thalami.
Doing an EEG
• 30 minutes to one hour.
• Patient hooked up to the machine, gel on
scalp and electrodes arranged in scalp in
whatever the favoured “montage” is.
• Recording is now done via computer and
subject to computer analysis.
• Patient may be subjected to stimulation, for
example flashing lights during recording,
asked to close or open eyes etc.
Alpha Rhythm
First one Berger saw
Seen when eyes are closed
and subject is relaxing
8-12Hz-dominant thalamic
rhythm
Dominant background rhythm
Anatomically occipital area
It’s a normal rhythm, should
always be there.
Not present under 3
Reduced by sleep, drowsiness,
eyes open.
Mu
Similar to alpha but in a
different place, nearly the
same frequency.
6-8Hz
Somatosensory area
Abolished by contralateral
movement and indeed even
thinking about movement
Main thing is not to get
confused about Mu-it’s not
that relevant.
Beta rhythm
12-30 Hz
Normal dominant rhythm
when awake
To pass an exam, be awake
(way of remembering)
Theta
4-7hz
Seen when drowsy, sleeping
Children
Delirium (not withdrawal)
Coma
Brain injury, epilepsy,
encephalitis etc.
Delta
0-4hz
High amplitude
Dominant rhythm in young children
Stage 3 and 4 sleep
Otherwise always pathological in
adults.
Delta =death
To recap
Other waves
• There are other waves which include lambda,
V waves, POSTs (posterior occipital sharp
waves) but they will not be asked in any
psychiatric exam.
• Focus is alpha,beta,theta and delta
Normal EEG
Abnormal EEG findings
Delirium: In general the EEG
gets slow, theta and delta,
alpha reduced.
Hepatic encephalopathy:
slowing and triphasic waves.
Old variant CJD: triphasic
waves and slow
TLE: temporal lobe rhythmic
discharge and spikes
Dementia: Alzheimer’s and
others, in general slowing,
loss of alpha and in
Alzhzimer’s spikes
Epilepsy
Remember 2 basic types of
epilepsy
Idiopathic generalised
epilepsy- these are nearly
always associated with
polyspike and wave,
classically petit malchildhood absence attacks
3-4 hz per minute.
Focal: focal spikes, most
commonly originate from
temporal areas, ergo
rhythmic temporal slowing
and spikes.
Psychiatry and the EEG
• Why would a psychiatrist order an EEG?
Epilepsy
• Useful when epilepsy suspected.
• Insufficient on its own, remember epilepsy is a
clinical diagnosis.
• EEG telemetry is diagnostic for non epileptic
attack disorder
• When suspecting epilepsy related psychiatric
disturbance
• Forced normalisation/ alternative psychosis, if
you believe in it.
Delirium versus catatonia/psychogenic
mutism
• Very useful for diagnosis of delirium,
widespread slowing will occur in delirium or
other causes of stupor, if psychogenic the EEG
will be normal.
• Sometimes types of delirium, withdrawal from
alcohol and benzodiazepines is a fast EEG
state, lots of beta ( booze and benzos-beta)
Dementia versus pseudodementia
• Preservation of alpha is reassuring
• Some dementias have specific alterations for
example CJD periodic complexes/triphasic
waves
• Frontal dementias have relatively better EEGs
then alzheimer’s disease.
MCQs
Normal EEG
• Alpha is present in sleep
• Mu is increased by
movement.
• Beta is from 2-4hz
• Delta is always pathological
• Delta in a three year old
may be normal
• Spikes always indicate
epilepsy
Abnormal EEG findings
•
•
•
•
•
•
•
Delirium tremens has a slow EEG
Delirium from hyponatremia has
prominent delta
CJD has periodic
complexes/triphasic waves
Hepatic encephalopathy can look
similar to CJD
Temporal lobe spikes with frequent
feelings of déjà vu suggest TLE
3-4 hz polyspike and wave in a six
year old child suggest absence
seizures.
Alzheimer’s is associated with loss
of alpha rhythm and development
of a slow EEG
EEG MCQs
Normal EEG
• Theta-4-7hz
• Delta-0-4hz
• Beta-12-30hz
• Alpha-8-12hz
• Alpha-dominant posterior
• Varies over 24 hours
Abnormal EEG
• Herpes encephalitis is
associated with PLEDs
• There are EEG findings in
depression.
• There are EEG findings in
schizophrenia
• A normal EEG in an abnormal
patient is a hard sign.
• An abnormal EEG in a normal
patient is a hard sign.
Sleep and consciousness
•
•
•
•
•
•
•
Overview
Consciousness
Anatomy
Biochemistry
Normal sleep
Abnormal sleep
MCQs
Consciousness
• Normal consciousness,
we all know what that is
but try defining it!
• Awake, fully aware of
environment and
oneself.
• 2 things arousal and
cognition.
• Abnormal
consciousness
• Coma
• Stupor
• Torpor
• Lethargy
• Akinetic mutism
• Catatonia
• Locked in syndrome
Consciousness and the ARAS
Structures involved
• Ascending reticular activating system
• Thalamus bilaterally and particulary
intalaminar nuclei of thalami
• Hypothalamus
• Thalamic frontal connections
Consciousness
Aroual
• ARAS and thalami
Cognitive
• Cerebral hemispheres
Basic neurochemistry
Wake promoting
• Noradrenaline
• Ach
• Histamine
• Dopamine
Sleep promoting
• Melatonin
• Gaba
• Note-hypocretins
• Hypocretin 1 and hyopcretin
2 human dorsolateral
hyopthalamus-important for
wake promoting systems,
loss is associated with
narcolepsy
Sleep
Non rapid eye movement sleep
• Stage 1 and 2=light sleep
• Stage 3 and 4=slow wave
sleep (SWS)
• SWS needed for CNS repair
and declarative memory
Rapid eye movement sleep
• Cycles every night
• Skeletal atonia
• Dreaming
• Physiological arousal, pe
HT-hemispheresdiencephalon-ARAS
• In bed at 10PM with
improving book and hot
chocolate.
• Lights out 10.20PM
• Good sleep by 11PM
• Wake up 7am
Changes in EEG, EOG and
EMG-head, eyes and
muscles.
• What happens?
Sleep
Poorly understood
Drive via suprachiasmatic
nucleus of hypothalamus
4-wakefullness, light sleep,
SWS/deep sleep and REM
Sleep
Stage 1, alpha goes, theta
appears, rolling eye
movements
Stage 2, sleep spindles, bursts
of 14-16hz and K complexes
Stage 3 and stage 4, lots of
delta, slow heart, lowered BP,
relaxatoin, reduction of BMR
by 70%
REM: desynchronisagtion of
EEG, saccadic eye
movements, atonia, limbic
regions are active
First rem after 60-90 minutes,
cycle continues and quantity
of REM increases whilst
amount of SWS reduces
Disorders of sleep, firstly is it abnormal
or not?
• Firstly consider age of patient, older patients
commonly have six EEG defined arousals per
night.
• Periodic limb movements occur in up to 1/3 of
elderly population
• Children do not have a normal EEG or sleep
wake cycle or indeed anything!
• Occasional sleep starts and abnormalities of
sleep are common in normal people
Hypersomnias
Excessive daytime
sleepiness
5% of population
Generally secondary to
poor sleep at night
If you sleep badly at night,
then you will make it up
during the day.
Obstructive Sleep Apnoea
Central obesity
Poor oropharyngeal
muscle tone
Rugby forward physiques
Snoring
Apneic attacks
Headaches
Fatigue
Loss of libido
Poor concentration
Treat, weight loss, surgery,
CPAP
narcolepsy
1:2000
Onset adolescence
Loss of HT neurons
containing hypocretin
Clinically:tetrad
Daytime sleep attacks
Cataplexy- can be partial or
total, loss of muscle tone
with high emotion
Sleep paralysis
Hypnogogic and
hypnopompic
hallucinations
Narcolepsy 2
REM sleep gone wild!
Autoimmune hypothesis
Strong association with
HLA DQB1 0602
CSF shows reduced
hypocretin, not quite
diagnostic
Diagnosis: history, MSLT
which shows rapid entry
into REM, HLA typing and
rarely CSF
Treatment
• Daytime sleepiness, cataplexy and nocturnal
sleep
• Planned naps
• Wake promotion: modafinil and speed.
• Cataplexy: venlafaxine and clomipramine
• Nocturnal disruption:clonazepam
Idiopathic hypersomnia
•
•
•
•
•
•
•
1:20,000
Daytime napping
Generally inattentive during day
Sleep good at night as measured by hypnogram
Waking up is difficult
Mood disorders are common
On MSLT, deep non rem achieved quickly but not
rem which happens in narcolepsy
Klein-Levin
• Generally teenage boys
• Very rare
• Intermittent
hypersomnolence
• Cognitive disturbance
• Hyperphagia
• Hypersexuality
• 1-2 weeks and normal
between
• May last for a decade and
then resolve
spontaneously
Parasomnias
• Problems arising from sleep
• Sleep wake transition disorders
• Non REM or REM
Sleep wake transition problems
•
•
•
•
Hypnic jerks and sensory starts
Head banging “jacatio capitis nocturna”
Propiospinal myoclonus
Periodic limb movements of sleep, lower
limbs, foot dorsiflexion and then spreads over
about a second, every 20-40 seconds, happen
in 50% of elderly, greater then five per hour is
abnormal?,
Non REM
• Night terrors, confusional arousals and sleep walkingpartial arousal form deep sleep, SWS, stage 3 and stage
4.
• Memory for events is poor.
• May run in families
• Can occur in 6% of children
• Night terrors; sudden piercing scream, one hour into
sleep, terrible fear and total amnesia for event
• Confusional arousals; wake up briefly and stare around
• Sleepwalking; unknown what happens, semiarousal
from deep sleep
Sleepwalking
Non REM 2
• Sleep related eating disorder; nocturnal binge
eating disorder
• Violence or sexual assault during deep sleep
parasomnias has been reported.
• Rarely nocturnal visual hallucinations in the
elderly
REM parasomnias
• Nightmares
• REM sleep paralysis
• REM sleep behaviour disorder, note “oneiric”
behaiour, 87% men, onset in mid 60s,
frequently associated with violent behavior,
dreams of being attacked etc, frequently
associated with synucleinopathies, Parkinson’s
disease and LBD, treatment: move out
partner, clonazepam
Nightmares
Psychiatric disorders and sleep
• Schizophrenia-short REM latency probably
secondary to SWS deficits.
• Restless legs syndrome is common in anxiety
disorders
• GAD associated with insomnia
• PTSD and nightmares, more REM
• Dementias: broken sleep pattern,
suprachiasmatic nucleus gone.
MCQs
In normal sleep
• REM occurs within 30 minutes
• Stage 1 and 2 have rolling eye
movements
• Stage four has mainly theta
and some delta
• REM is associated with atonia
• Stage 3 and 4 is called SWS
• SWS is important for memory
In hypersomnias
• HLA typing may be
important
• Losing weight is a common
treatment
• CPAP is useful for some
patients
• Addiction to stimulants can
be a problem
• Men are more affected
them women
MCQs
narcolepsy
REM sleep parasomnias
Prevalence of 1:200
Has association with HLA DR2 405
Is always associated with
cataplexy
Can cause sleep paralysis
Can cause vivid hallucinations
Responds to treatment with
modafinil
An afternoon nap may be a
legitimate treatment
• Night terrrors are a rem
problem arising from dreams
• REM sleep parasomnias have a
link with alpha synuclein
• In PTSD nightmares occur in
50% of patients
• Sleepwalking is common
• Can be reproduced by
lesioning in cats
• Pontine stroke can cause
bizare dreams and visual
hallucinations
MCQs
In schizophrenia
•
•
•
•
•
Clear EEG findings
Reduction of alpha rhythm
Sleep is normal
Reduction of SWS
Medications may interfere
with sleep
• Medications are generally
sedating
• Some medications used may
cause gross EEG abnormalities
In GAD
• The inter rater reliability is
high.
• Sleep disorder is comon.
• In depression
• Insomnia can be used as a
treatment
• EMW is associated with
cortisol hypersecretion